由FXII活化而启动。当血管受损，内膜下胶原纤维暴露时，可激活XII为

It is activated by FXII activation. When blood vessels are damaged and collagen fibers under the intima are exposed, XII can be activated to XIIa, which in turn activates XI to XIa. XIa activates Ⅸa in the presence of Ca2+, and IXa forms a complex with activated Ⅷa, PF3, and Ca2+ to further activate X. The factors involved in coagulation in the above process are all present in the plasma in the blood vessel, so it is called the endogenous coagulation pathway. Due to the presence of factor Ⅷa, the rate of activation of X by Ⅸa can be accelerated by 200,000 times

Launched by FXII activation. When blood vessels are damaged and collagen fibers in the lining are exposed, XII can be activated as XII, which in turn activates XI as XIa. XIa activates IX.a when Ca2 plus exists, and IX.a is further activated X with the activated VIII.a, PF3, Ca2 plus composite. The factors involved in clotting in the above process are present in the plasma of blood vessels, so it is named endogenous clotting pathway. Because of the existence of factor VIII.a, ix a activation of X speed up by 200,000 times, so factor VIII lack of endogenous clotting pathway disorder, slight injury can cause bleeding more than, clinically known as Haheitomopathy A haemophilia

Activated by FXII. When the blood vessels are damaged and the subintimal collagen fibers are exposed, XIIa can be activated, and then XIIa can be activated. Xia activates ⅸ a in the presence of Ca2 +, and ⅸ a reacts with the activated Ⅷ a, PF3 and Ca2 + to form complex to further activate X. All the factors involved in the coagulation process are present in the blood plasma, so they are called endogenous coagulation pathway. Due to the existence of factor Ⅷ a, the activation rate of ⅸ a can be increased by 200000 times. Therefore, the lack of factor Ⅷ can cause the disorder of endogenous coagulation pathway, and slight damage can lead to bleeding. It is called hemophilia A a clinically<br>